Extending the radius of family-centered care in the pediatric cardiac intensive care unit through virtual rounding.

Background: The arrival of COVID-19 brought urgent limitation of visitation in hospitals across the country. Family-centered care and its delivery rapidly changed and left the family behind-unable to actively participate in their loved one's care.

Local Problem: A southeastern academic medical center pediatric cardiac intensive care unit (PCICU) needed to augment family-centered medical rounds when parents could not be at the bedside.

The effect of intraoperative methadone during pediatric cardiac surgery on postoperative opioid requirements.

Background: Pain control in pediatric patients undergoing cardiac surgery presents a unique challenge. Postoperatively, many of these patients require long-term opioid infusions and sedation leading to need for prolonged weaning from opioids and longer hospital stays. We hypothesized that intravenous methadone as the sole opioid in children having cardiac surgery with cardiopulmonary bypass would improve perioperative pain control and decrease overall perioperative use of opioid analgesics and sedatives.

Outcomes associated with peripherally inserted central catheters in hospitalised children: a retrospective 7-year single-centre experience.

Objectives: The use of peripherally inserted central catheters (PICCs) are an integral part of caring for hospitalised children. We sought to estimate the incidence of and identify the risk factors for complications associated with PICCs in an advanced registered nurse practitioners (ARNP)-driven programme.

Design: Retrospective cohort study.

Circuit oxygenator contributes to extracorporeal membrane oxygenation-induced hemolysis.

Hemolysis can occur as a consequence of extracorporeal membrane oxygenation (ECMO) and is associated with increased mortality and morbidity. Shear stress generated by flow through the circuit and oxygenator is believed to cause ECMO-induced hemolysis. We hypothesize that either a smaller dimension oxygenator or an in-line hemofilter will increase ECMO-associated hemolysis.

Cardiopulmonary bypass is associated with hemolysis and acute kidney injury in neonates, infants, and children*.

Objectives: This pilot study assesses the degree of hemolysis induced by cardiopulmonary bypass and determines its association with acute kidney injury in pediatric patients. Further, it evaluates the degree to which the use of urinary biomarkers neutrophil gelatinase-associated lipocalin and cystatin C correlate with the presence of acute kidney injury and hemolysis following cardiopulmonary bypass.

Design: Prospective observational study.

Sequestration of mitochondrial iron by silica particle initiates a biological effect.

Inhalation of particulate matter has presented a challenge to human health for thousands of years. The underlying mechanism for biological effect following particle exposure is incompletely understood. We tested the postulate that particle sequestration of cell and mitochondrial iron is a pivotal event mediating oxidant generation and biological effect.

Transfusion-related biologic effects and free hemoglobin, heme, and iron.

Background: Red blood cell (RBC) transfusion is common in intensive care unit (ICU) patients and is associated with complications that appear related to the duration of blood storage. We hypothesize that hemolysis of stored RBCs results in increases in the availability of non-heme-bound iron, which inhibits macrophage activation.

Study Design And Methods: RBCs were sampled at multiple time points to evaluate hemolysis and iron release.

Disruption of iron homeostasis in mesothelial cells after talc pleurodesis.

The mechanism for biological effects after exposure to particles is incompletely understood. One postulate proposed to explain biological effects after exposure to particles involves altered iron homeostasis in the host. The fibro-inflammatory properties of mineral oxide particles are exploited therapeutically with the instillation of massive quantities of talc into the pleural space, to provide sclerosis.

Hepcidin expression in human airway epithelial cells is regulated by interferon-γ.

Background: Hepcidin serves as a major regulator of systemic iron metabolism and immune function. Airway epithelial cells have an extensive interface with the environment, and so must be able to respond locally to the presence of particulates, infection, and inflammation. Therefore, we hypothesized that hepcidin is expressed in airway epithelial cells and is regulated by early phase cytokines.

Iron overload following red blood cell transfusion and its impact on disease severity.

Transfusion of red blood cells can be a life-saving therapy both for patients with chronic anemias and for those who are critically ill with acute blood loss. However, transfusion has been associated with significant morbidity. Chronic transfusion results in accumulation of excess iron that surpasses the binding capacity of the major iron transport protein, transferrin.

Iron accumulation in bronchial epithelial cells is dependent on concurrent sodium transport.

Airway epithelial cells prevent damaging effects of extracellular iron by taking up the metal and sequestering it within intracellular ferritin. Epithelial iron transport is associated with transcellular movement of other cations including changes in the expression or activity of Na, K-ATPase and epithelial Na(+) channel (ENaC). Given this relationship between iron and Na(+), we hypothesized that iron uptake by airway epithelial cells requires concurrent Na(+) transport.

Lung injury after ozone exposure is iron dependent.

We tested the hypothesis that oxidative stress and biological effect after ozone (O3) exposure are dependent on changes in iron homeostasis. After O3 exposure, healthy volunteers demonstrated increased lavage concentrations of iron, transferrin, lactoferrin, and ferritin. In normal rats, alterations of iron metabolism after O3 exposure were immediate and preceded the inflammatory influx.

Iron homeostasis in the lung.

Iron is essential for many aspects of cellular function. However, it also can generate oxygen-based free radicals that result in injury to biological molecules. For this reason, iron acquisition and distribution are tightly regulated.

Duodenal cytochrome b: a novel ferrireductase in airway epithelial cells.

Catalytically active iron in the lung causes oxidative stress and promotes microbial growth that can be limited by intracellular sequestration of iron within ferritin. Because cellular iron uptake requires membrane ferrireductase activity that in the gut can be provided by duodenal cytochrome b (Dcytb), we sought Dcytb in the lung to test the hypothesis that it contributes to epithelial iron regulation by reducing Fe(3+) for cellular iron transport. Dcytb expression was found in respiratory epithelium in vitro and in vivo and was responsive to iron concentration.

The iron cycle and oxidative stress in the lung.

Iron is critical for many aspects of cellular function, but it can also generate reactive oxygen species that can damage biological macromolecules. To limit oxidative stress, iron acquisition and its distribution must be tightly regulated. In the lungs, which are continuously exposed to the atmosphere, the risk of oxidative damage is particularly high because of the high oxygen concentration and the presence of significant amounts of catalytically active iron in atmospheric particulates.

Superoxide-dependent iron uptake: a new role for anion exchange protein 2.

Lung cells import iron across the plasma membrane as ferrous (Fe2+) ion by incompletely understood mechanisms. We tested the hypothesis that human bronchial epithelial (HBE) cells import non-transferrin-bound iron (NTBI) using superoxide-dependent ferri-reductase activity involving anion exchange protein 2 (AE2) and extracellular bicarbonate (HCO3-). HBE cells that constitutively express AE2 mRNA by reverse transcriptase-polymerase chain reaction and AE2 protein by Western analysis avidly transported NTBI after exposure to either Fe2+ or Fe3+, but reduction of Fe3+ to Fe2+ was first required.

Oxidative stress activates anion exchange protein 2 and AP-1 in airway epithelial cells.

Anion exchange protein 2 (AE2) is a membrane-bound protein that mediates chloride-bicarbonate exchange. In addition to regulating intracellular pH and cell volume, AE2 exports superoxide (O.) to the extracellular matrix in an HCO-dependent process.